INPUT on possible article ????

[MuscleScience]

I have this theory that stacking two or more compounds with different binding affinities for the AR will compete with each other. Thus causing one compounds effects to effectively be blocked or reduced. This is the how compounds like tamoxifen citrate effectively block estrogens effects on the ER.

[magic32]

the answer is...
A) 1/3

LOL, as any Hitchhiker's Guide knowledgeable person knows the answer is "42".

Ill get back to you on that...

All kidding aside this is a very serious question with some significant ramifications, peripheral to which happens to be the answer to MS’s (I always liked this guy) present & extremely apt question:

I have this theory that stacking two or more compounds with different binding affinities for the AR will compete with each other. Thus causing one compounds effects to effectively be blocked or reduced. This is the how compounds like tamoxifen citrate effectively block estrogens effects on the ER.

There really is a very rational and comprehensible answer to both of our questions which has to do the two metabolites of the steroid hormones progesterone and deoxycorticosterone, 3 alpha-hydroxy-5 alpha-dihydroprogesterone and 3 alpha, 5 alpha-tetrahydrodeoxycorticosterone, are potent barbiturate-like ligands of the gamma-aminobutyric acid (GABA) receptor-chloride ion channel complex. At concentrations between 10(-7) and 10(-5)M both steroids inhibited binding of the convulsant t-butylbicyclophosphorothionate to the GABA-receptor complex and increased the binding of the benzodiazepine flunitrazepam; they also stimulated chloride uptake (as measured by uptake of 36Cl-) into isolated brain vesicles, and potentiated the inhibitory actions of GABA in cultured rat hippocampal and spinal cord neurons. These data may explain the ability of certain steroid hormones (and other contraindicative hormone related drugs like SERMs and AIs) to rapidly alter neuronal excitability and may provide a mechanism for the inhibiting actions of numerous naturally occurring bodiliy chemicals as well as, both synthetic anesthetic & "YES" believe it or not, similarly reactive anabolic steroid synthesis.

Merc,

Should you be so inclined, here are some of the central resources...

http://www.pubmedcentral.nih.gov/art...?artid=2042897
http://www.ncbi.nlm.nih.gov/pubmed/15282269
http://www.ncbi.nlm.nih.gov/pubmed/16702996
http://www.ncbi.nlm.nih.gov/pubmed/2598927
http://www.ncbi.nlm.nih.gov/pubmed/2888123
http://www.ncbi.nlm.nih.gov/pubmed/2445967

[MuscleScience]

LOL, as any Hitchhiker's Guide knowledgeable person knows the answer is "42".

All kidding aside this is a very serious question with some significant ramifications, peripheral to which happens to be the answer to MS’s (I always liked this guy) present & extremely apt question:

There really is a very rational and comprehensible answer to both of our questions which has to do the two metabolites of the steroid hormones progesterone and deoxycorticosterone, 3 alpha-hydroxy-5 alpha-dihydroprogesterone and 3 alpha, 5 alpha-tetrahydrodeoxycorticosterone, are potent barbiturate-like ligands of the gamma-aminobutyric acid (GABA) receptor-chloride ion channel complex. At concentrations between 10(-7) and 10(-5)M both steroids inhibited binding of the convulsant t-butylbicyclophosphorothionate to the GABA-receptor complex and increased the binding of the benzodiazepine flunitrazepam; they also stimulated chloride uptake (as measured by uptake of 36Cl-) into isolated brain vesicles, and potentiated the inhibitory actions of GABA in cultured rat hippocampal and spinal cord neurons. These data may explain the ability of certain steroid hormones (and other contraindicative hormone related drugs like SERMs and AIs) to rapidly alter neuronal excitability and may provide a mechanism for the inhibiting actions of numerous naturally occurring bodiliy chemicals as well as, both synthetic anesthetic & "YES" believe it or not, similarly reactive anabolic steroid synthesis.

Merc,

Should you be so inclined, here are some of the central resources...

http://www.pubmedcentral.nih.gov/art...?artid=2042897
http://www.ncbi.nlm.nih.gov/pubmed/15282269
http://www.ncbi.nlm.nih.gov/pubmed/16702996
http://www.ncbi.nlm.nih.gov/pubmed/2598927
http://www.ncbi.nlm.nih.gov/pubmed/2888123
http://www.ncbi.nlm.nih.gov/pubmed/2445967

I bet if you and I were on pubmed at the same time we would crash their servers....LOL

Nice writeup btw!

[Merc.]

LOL, as any Hitchhiker's Guide knowledgeable person knows the answer is "42".

All kidding aside this is a very serious question with some significant ramifications, peripheral to which happens to be the answer to MS’s (I always liked this guy) present & extremely apt question:

There really is a very rational and comprehensible answer to both of our questions which has to do the two metabolites of the steroid hormones progesterone and deoxycorticosterone, 3 alpha-hydroxy-5 alpha-dihydroprogesterone and 3 alpha, 5 alpha-tetrahydrodeoxycorticosterone, are potent barbiturate-like ligands of the gamma-aminobutyric acid (GABA) receptor-chloride ion channel complex. At concentrations between 10(-7) and 10(-5)M both steroids inhibited binding of the convulsant t-butylbicyclophosphorothionate to the GABA-receptor complex and increased the binding of the benzodiazepine flunitrazepam; they also stimulated chloride uptake (as measured by uptake of 36Cl-) into isolated brain vesicles, and potentiated the inhibitory actions of GABA in cultured rat hippocampal and spinal cord neurons. These data may explain the ability of certain steroid hormones (and other contraindicative hormone related drugs like SERMs and AIs) to rapidly alter neuronal excitability and may provide a mechanism for the inhibiting actions of numerous naturally occurring bodiliy chemicals as well as, both synthetic anesthetic & "YES" believe it or not, similarly reactive anabolic steroid synthesis.

Merc,

Should you be so inclined, here are some of the central resources...

http://www.pubmedcentral.nih.gov/art...?artid=2042897
http://www.ncbi.nlm.nih.gov/pubmed/15282269
http://www.ncbi.nlm.nih.gov/pubmed/16702996
http://www.ncbi.nlm.nih.gov/pubmed/2598927
http://www.ncbi.nlm.nih.gov/pubmed/2888123
http://www.ncbi.nlm.nih.gov/pubmed/2445967

Sorry for the delayed response .. I have had very little time to post on the board( it has been a busy few weeks)..

Very interesting Magic ...... This is going to give us some possible in site as to the cause of aggression when using certain AAS compounds..

As I am sure you know .. GABA regulates serotonin and the catacholmines ( L-dopa, norepinephrine , adrenaline )..

So the inhibition of GABA would have an effect on chemicals called serotonergic amines ( in the brain) which would decrease brain serotonin( which could/would cause aggression) .. As well as have a negative effect on dopamine ( which allows one to feel joy , and have energy)..

Since there aren't really any valid studies using compounds ( like tren, in humans) I think this could be a very good article and could give some great in site about neurotransmitters - increased aggression , depression and anxiety caused by GABA inhibition while using certain AAS ..


Merc.